Paroxysmal Sympathetic Hyperactivity After Severe Traumatic Brain Injury in Children: Prevalence, Risk Factors, and Outcome.

OBJECTIVE: To describe paroxysmal sympathetic hyperactivity in pediatric patients with severe traumatic brain injury using the new consensus definition, the risk factors associated with developing paroxysmal sympathetic hyperactivity, and the outcomes associated with paroxysmal sympathetic hyperactivity. DESIGN: Retrospective cohort study. SETTING: Academic children's hospital PICU. PATIENTS: All pediatric patients more than 1 month and less than 18 years old with severe traumatic brain injury between 2000 and 2016. We excluded patients if they had a history of five possible confounders for paroxysmal sympathetic hyperactivity diagnosis or if they died within 24 hours of admission for traumatic brain injury. MEASUREMENTS AND MAIN RESULTS: Our primary outcome was PICU mortality. One hundred seventy-nine patients met inclusion criteria. Thirty-six patients (20%) had at least eight criteria and therefore met classification of "likelihood of paroxysmal sympathetic hyperactivity." Older age was the only factor independently associated with developing paroxysmal sympathetic hyperactivity (odds ratio, 1.08; 95% CI, 1.00-1.16). PICU mortality was significantly lower for those with paroxysmal sympathetic hyperactivity compared with those without paroxysmal sympathetic hyperactivity (odds ratio, 0.08; 95% CI, 0.01-0.52), but PICU length of stay was greater in those with paroxysmal sympathetic hyperactivity (odds ratio, 4.36; 95% CI, 2.94-5.78), and discharge to an acute care or rehabilitation setting versus home was higher in those with paroxysmal sympathetic hyperactivity (odds ratio, 5.59; 95% CI, 1.26-24.84; odds ratio, 5.39; 95% CI, 1.87-15.57, respectively). When paroxysmal sympathetic hyperactivity was diagnosed in the first week of admission, it was not associated with discharge disposition. CONCLUSIONS: Our study suggests that the rate of paroxysmal sympathetic hyperactivity in patients with severe traumatic brain injury is higher than previously reported. Older age was associated with an increased risk for developing paroxysmal sympathetic hyperactivity, but severity of the trauma and the brain injury were not. For survivors of severe traumatic brain injury beyond 24 hours who developed paroxysmal sympathetic hyperactivity, there was a lower PICU mortality but also greater PICU length of stay and a lower likelihood of discharge home from the admitting hospital, suggesting that functional outcome in survivors with paroxysmal sympathetic hyperactivity is worse than survivors without paroxysmal sympathetic hyperactivity.

CXCL1/CXCL8 (GROα/IL-8) in human diabetic ketoacidosis plasma facilitates leukocyte recruitment to cerebrovascular endothelium in vitro.

Diabetic ketoacidosis (DKA) in children is associated with intracranial vascular complications, possibly due to leukocyte-endothelial interactions. Our aim was to determine whether DKA-induced inflammation promoted leukocyte adhesion to activated human cerebrovascular endothelium. Plasma was obtained from children with type 1 diabetes either in acute DKA or in an insulin-controlled state (CON). Plasma concentrations of 21 inflammatory analytes were compared between groups. DKA was associated with altered circulating levels of ↑CXCL1 (GROα), ↑CXCL8 (IL-8), ↑IL-6, ↑IFNα2, and ↓CXCL10 (IP-10) compared with CON. These plasma analyte measurements were then used to create physiologically relevant cytokine mixtures (CM). Human cerebral microvascular endothelial cells (hCMEC/D3) were stimulated with either plasma (DKA-P or CON-P) or CM (DKA-CM or CON-CM) and assessed for polymorphonuclear leukocyte (PMN) adhesion. Stimulation of hCMEC/D3 with DKA-P or DKA-CM increased PMN adhesion to hCMEC/D3 under "flow" conditions. PMN adhesion to hCMEC/D3 was suppressed with neutralizing antibodies to CXCL1/CXCL8 or their hCMEC/D3 receptors CXCR1/CXCR2. DKA-P, but not DKA-CM, initiated oxidative stress in hCMEC/D3. Expression of ICAM-1, VCAM-1, and E-selectin were unaltered on hCMEC/D3 by either DKA-P or DKA-CM. In summary, DKA elicits inflammation in children associated with changes in circulating cytokines/chemokines. Increased CXCL1/CXCL8 instigated PMN adhesion to hCMEC/D3, possibly contributing to DKA-associated intracranial vascular complications.

Brain injury biomarkers as outcome predictors in pediatric severe traumatic brain injury.

BACKGROUND: To systematically review the literature on brain injury biomarkers, defined as any injury biomarker detected in cerebrospinal fluid (CSF) or blood injury biomarkers primarily expressed in the brain parenchyma, to determine outcome prediction in pediatric severe traumatic brain injury (sTBI). METHODS: A search of MEDLINE(®), EMBASE(®), PsycINFO(®), Pubmed(®), and the Cochrane Database, as well as grey literature sources, personal contacts, hand searches, and reference lists. The search terms used were traumatic brain injury, biomarkers, prognosis, and children. No language, publication type, or publication date restrictions were imposed. All articles were critically reviewed by two clinicians independently. RESULTS: A total of 7,150 articles were identified initially with 16 studies identified for review. Eighteen different biomarkers were examined; 11 in CSF and 7 in blood. Outcomes assessed included either in-hospital mortality or functional state (hospital discharge, 3-months or 6-months; Glasgow Outcome Scale or Pediatric Cerebral Performance Category). Significant correlations were established between sTBI outcomes and various biomarkers in CSF (IL-6, IL-8, IL-1ß, S100ß, NGF, NSE, DCX, ET-1, HMGB-1, cytochrome C) and blood (GFAP, NF-H, UCH-L1, SBDP-145, leptin). Mixed results were obtained for blood S100ß. Outcome did not correlate with several biomarkers in either CSF (BDNF, GDNF, α-Syn) or blood (NSE, MBP). The Class of Evidence was considered II in 1 study and III in the remaining 15 studies. CONCLUSIONS: Based on the status of current sTBI biomarker research, we recommend that future research should be directed at both novel biomarker discovery and validation of biomarker panels in large, well-designed longitudinal studies.

Subarachnoid hemorrhage prevalence and its association with short-term outcome in pediatric severe traumatic brain injury.

BACKGROUND: Subarachnoid hemorrhage (SAH) is an independent prognostic indicator of outcome in adult severe traumatic brain injury (sTBI). There is a paucity of investigations on SAH in pediatric sTBI. The goal of this study was to determine in pediatric sTBI patients SAH prevalence, associated factors, and its relationship to short-term outcome. METHODS: We retrospectively analyzed 171 sTBI patients (pre-sedation GCS ≤8 and head MAIS ≥4) who underwent CT head imaging within the first 24 h of hospital admission. Data were analyzed with both univariate and multivariate techniques. RESULTS: SAH was found in 42 % of sTBI patients (n = 71/171), and it was more frequently associated with skull fractures, cerebral edema, diffuse axonal injury, contusion, and intraventricular hemorrhage (p < 0.05). Patients with SAH had higher Injury Severity Scores (p = 0.032) and a greater frequency of fixed pupil(s) on admission (p = 0.001). There were no significant differences in etiologies between sTBI patients with and without SAH. Worse disposition occurred in sTBI patients with SAH, including increased mortality (p = 0.009), increased episodes of central diabetes insipidus (p = 0.002), greater infection rates (p = 0.002), and fewer ventilator-free days (p = 0.001). In sTBI survivors, SAH was associated with increased lengths of stay (p < 0.001) and a higher level of care required on discharge (p = 0.004). Despite evidence that SAH is linked to poorer outcomes on univariate analyses, multivariate analysis failed to demonstrate an independent association between SAH and mortality (p = 0.969). CONCLUSION: SAH was present in almost half of pediatric sTBI patients, and it was indicative of TBI severity and a higher level of care on discharge. SAH in pediatric patients was not independently associated with increased risk of mortality.

Hyperosmolar hyperglycemic state without ketosis in a toddler with type 1 diabetes.

We present a thin toddler whose initial presentation with type 1 diabetes was hyperglycemic hyperosmolar syndrome without diabetic ketoacidosis after ingestion of copious quantities of high-sugar beverages. Increasing consumption of high-sugar beverages may make this presentation of type 1 diabetes mellitus more common. Emergency care physicians must be aware of this potential clinical constellation in the very young, as management differs significantly from that accepted for diabetic ketoacidosis in children.

Central diabetes insipidus in pediatric severe traumatic brain injury.

OBJECTIVES: To determine the occurrence rate of central diabetes insipidus in pediatric patients with severe traumatic brain injury and to describe the clinical, injury, biochemical, imaging, and intervention variables associated with mortality. DESIGN: Retrospective chart and imaging review. SETTING: Children's Hospital, level 1 trauma center. PATIENTS: Severely injured (Injury Severity Score ≥ 12) pediatric trauma patients (>1 month and <18 yr) with severe traumatic brain injury (presedation Glasgow Coma Scale ≤ 8 and head Maximum Abbreviated Injury Scale ≥ 4) that developed acute central diabetes insipidus between January 2000 and December 2011. MEASUREMENTS AND MAIN RESULTS: Of 818 severely injured trauma patients, 180 had severe traumatic brain injury with an overall mortality rate of 27.2%. Thirty-two of the severe traumatic brain injury patients developed acute central diabetes insipidus that responded to desamino-8-D-arginine vasopressin and/or vasopressin infusion, providing an occurrence rate of 18%. At the time of central diabetes insipidus diagnosis, median urine output and serum sodium were 6.8 ml/kg/hr (interquartile range = 5-11) and 154 mmol/L (interquartile range = 149-159), respectively. The mortality rate of central diabetes insipidus patients was 87.5%, with 71.4% declared brain dead after central diabetes insipidus diagnosis. Early central diabetes insipidus onset, within the first 2 days of severe traumatic brain injury, was strongly associated with mortality (p < 0.001), as were a lower presedation Glasgow Coma Scale (p = 0.03), a lower motor Glasgow Coma Scale (p = 0.01), an occurrence of fixed pupils (p = 0.04), and a prolonged partial thromboplastin time (p = 0.04). Cerebral edema on the initial computed tomography, obtained in the first 24 hrs after injury, was the only imaging finding associated with death (p = 0.002). Survivors of central diabetes insipidus were more likely to have intracranial pressure monitoring (p = 0.03), have thiopental administered to induce coma (p = 0.04) and have received a decompressive craniectomy for elevated intracranial pressure (p = 0.04). CONCLUSIONS: The incidence of central diabetes insipidus in pediatric patients with severe traumatic brain injury is 18%. Mortality was associated with early central diabetes insipidus onset and cerebral edema on head computed tomography. Central diabetes insipidus nonsurvivors were less likely to have received intracranial pressure monitoring, thiopental coma and decompressive craniectomy.

Pediatric severe traumatic brain injury mortality prediction determined with machine learning-based modeling.

INTRODUCTION: Severe traumatic brain injury (sTBI) is a leading cause of mortality in children. As clinical prognostication is important in guiding optimal care and decision making, our goal was to create a highly discriminative sTBI outcome prediction model for mortality. METHODS: Machine learning and advanced analytics were applied to the patient admission variables obtained from a comprehensive pediatric sTBI database. Demographic and clinical data, head CT imaging abnormalities and blood biochemical data from 196 children and adolescents admitted to a tertiary pediatric intensive care unit (PICU) with sTBI were integrated using feature ranking by way of a forest of randomized decision trees, and a model was generated from a reduced number of admission variables with maximal ability to discriminate outcome. RESULTS: In total, 36 admission variables were analyzed using feature ranking with variable weighting to determine their predictive importance for mortality following sTBI. Reduction analysis utilizing Borata feature selection resulted in a parsimonious six-variable model with a mortality classification accuracy of 82%. The final admission variables that predicted mortality were: partial thromboplastin time (22%); motor Glasgow Coma Scale (21%); serum glucose (16%); fixed pupil(s) (16%); platelet count (13%) and creatinine (12%). Using only these six admission variables, a t-distributed stochastic nearest neighbor embedding algorithm plot demonstrated visual separation of sTBI patients that lived or died, with high mortality predictive ability of this model on the validation dataset (AUC = 0.90) which was confirmed with a conventional area-under-the-curve statistical approach on the total dataset (AUC = 0.91; P < 0.001). CONCLUSIONS: Machine learning-based modeling identified the most clinically important prognostic factors resulting in a pragmatic, high performing prognostic tool for pediatric sTBI with excellent discriminative ability to predict mortality risk with 82% classification accuracy (AUC = 0.90). After external multicenter validation, our prognostic model might help to guide treatment decisions, aggressiveness of therapy and prepare family members and caregivers for timely end-of-life discussions and decision making. LEVEL OF EVIDENCE: III; Prognostic.

Development of a Mortality Prediction Tool in Pediatric Severe Traumatic Brain Injury.

Severe traumatic brain injury (sTBI) is a leading cause of pediatric death, yet outcomes remain difficult to predict. The goal of this study was to develop a predictive mortality tool in pediatric sTBI. We retrospectively analyzed 196 patients with sTBI (pre-sedation Glasgow Coma Scale [GCS] score <8 and head Maximum Abbreviated Injury Scale (MAIS) score >4) admitted to a pediatric intensive care unit (PICU). Overall, 56 patients with sTBI (29%) died during PICU stay. Of the survivors, 88 (63%) were discharged home, and 52 (37%) went to an acute care or rehabilitation facility. Receiver operating characteristic (ROC) curve analyses of admission variables showed that pre-sedation GCS score, Rotterdam computed tomography (CT) score, and partial thromboplastin time (PTT) were fair predictors of PICU mortality (area under the curve [AUC] = 0.79, 0.76, and 0.75, respectively; p < 0.001). Cutoff values best associated with PICU mortality were pre-sedation GCS score <5 (sensitivity = 0.91, specificity = 0.54), Rotterdam CT score >3 (sensitivity = 0.84, specificity = 0.53), and PTT >34.5 sec (sensitivity = 0.69 specificity = 0.67). Combining pre-sedation GCS score, Rotterdam CT score, and PTT in ROC curve analysis yielded an excellent predictor of PICU mortality (AUC = 0.91). In summary, pre-sedation GCS score (<5), Rotterdam CT score (>3), and PTT (>34.5 sec) obtained on hospital admission were fair predictors of PICU mortality, ranked highest to lowest. Combining these three admission variables resulted in an excellent pediatric sTBI mortality prediction tool for further prospective validation.

Identification of adverse events in pediatric severe traumatic brain injury patients to target evidence-based prevention for increased performance improvement and patient safety.

INTRODUCTION: Trauma centres are required to continuously measure, evaluate and improve care. Severe traumatic brain injury (sTBI) patients are highly susceptible to adverse events (AE; unintended, potentially harmful events resulting from health care) due to their unstable condition requiring high risk interventions, multiple medications and invasive monitoring. Objectives were to describe: (1) a process for identifying AE in pediatric sTBI patients to identify safety risks, target and implement evidence-based prevention strategies; and (2) a tertiary care PICU's sTBI AE experience. METHODS: Merging databases, Trauma Registry with Adverse Events Management System, identified AE in patients. Details on the event location, type and severity of harm were combined with patient demographics, injury data, costs and outcomes in a cohort of 193 PICU sTBI patients (2000-15). Descriptive statistics and multivariate logistic regression were undertaken to describe AE, and their association with risk factors and outcomes. RESULTS: 103/193 sTBI patients (53%) suffered at least one AE. 238 AE occurred (1.23 AE/patient), with 30% of patients having 2+ AE. Most resulted in no harm (54%) with decubitus ulcers (15%) the most common AE. AE patients were more likely to be monitored for elevated ICP (p<0.001), with fewer ventilator-free days (p=0.015), longer LOS for PICU (11 vs. 3.5 days; p<0.001) and in-hospital (31 vs. 11 days; p<0.001) with higher median costs ($121,234 vs. $53,341; p=0.031). AE patients required a higher level of care on discharge (p=0.035). CONCLUSIONS: Merging databases is an effective practice to identify AE and safety risks in trauma populations. Utilizing this method, a PICU AE rate of 1.23 events per patient was found with TBI severity the most important factor to increase the odds of AE. AE represent performance improvement events, opportunities to optimize care, decrease costs, as well as improve outcomes, to ultimately improve patient safety in this vulnerable population.

Corrigendum to "Designing and evaluating an automated intravenous dosage medication calculation tool for reducing the time of stat medication administration in a pediatric emergency department" [Heliyon 6 (6) (June 2020) Article e04140].

[This corrects the article DOI: 10.1016/j.heliyon.2020.e04140.].

Designing and evaluating an automated intravenous dosage medication calculation tool for reducing the time of stat medication administration in a pediatric emergency department.

BACKGROUND: Urgent medications are regularly prescribed using the term "stat", which indicates that the medication should be administered within 30 min after it is ordered. However, many hospitals struggle to reliably administer stat medications within 30 min after they are ordered. This study involved developing and evaluating an automated intravenous dosage medication calculation tool (AIVDMCT) for reducing the time between the order and administration of stat medications to children at a pediatric emergency department (PED) in Saudi Arabia. METHODS: This prospective observational study evaluated data from before (June-December 2016) and after (June-December 2017) the AIVDMCT was implemented for high-risk medications in our PED. Patients were considered eligible if they were <14 years old, weighed <40 kg, and required stat intravenous (IV) medications at the PED of our tertiary care hospital. RESULTS: Implementation of the AIVDMCT significantly reduce the intervals between the time of order (TO) and the time of preparation (TP) (average time: 8.05 ± 3.42 min) and between the TP and the time of administration (TA) (average time: 3.74 ± 1.70 min). Furthermore, the interval from the TO to the TA was significantly reduced after the AIVDMCT was implemented (average time: 11.79 ± 4.48 min, P < 0.001). CONCLUSION: The AIVDMCT was associated with a significant reduction in the interval from the TO to the TA. This increased the proportion of stat medications that were delivered within the 30-min target window.

Basal skull fractures are associated with mortality in pediatric severe traumatic brain injury.

BACKGROUND: Basal skull fractures (BSFs) are caused by blunt force trauma, occurring in the temporal, occipital, sphenoid, and/or ethmoid bones. In pediatric severe traumatic brain injury (sTBI), there is a paucity of data on BSFs. Our goal was to investigate the BSF prevalence, anatomy, and association with short-term outcomes in pediatric sTBI. METHODS: We retrospectively reviewed all severely injured (Injury Severity Score ≥12) pediatric patients (aged <18 years) admitted to our hospital after experiencing an sTBI (Glasgow Coma Scale score ≤8 and head Abbreviated Injury Scale score ≥4). Neuroimaging for all sTBI patients was reviewed for skull fractures. Data were analyzed with both univariate and multivariate techniques. RESULTS: Of the 180 patients with sTBI, 47 had BSFs for a prevalence of 26% (69 BSFs in total; 16 sTBI patients had ≥2 BSFs). The squamous temporal bone was fractured most frequently (n=30/47 sTBI patients with BSFs). Patients with BSFs were heavier and had more facial injuries than those without (p < 0.05) but were similar in all other admission demographics, injury profiles, and clinical characteristics. Cerebrospinal fluid leak was found in 32% (n = 15 of 47) of BSF patients (otorrhea, n = 12; rhinorrhea, n = 1; otorrhea/rhinorrhea, n = 2; p < 0.001). Mortality, acute central diabetes insipidus, and fewer ventilator-free days were associated with BSFs (p < 0.005), whereas in sTBI survivors, BSFs were associated with longer lengths of stay (p < 0.05). Multiple logistic regression showed that BSFs were positively associated with the presence of subarachnoid hemorrhage (odds ratio [OR], 4.00; p = 0.001), contusion (OR, 2.48; p = 0.029), herniation (OR, 3.40; p = 0.037), and cerebral edema (OR, 2.30; p = 0.047) but negatively associated with diffuse axonal injury (OR, 0.20; p = 0.003). BSFs and mortality were strongly associated (OR, 6.87; p = 0.019). CONCLUSION: BSFs occurred in 26% of pediatric sTBI patients. The temporal bone was fractured in two thirds of sTBI patients with BSFs, and one third was associated with cerebrospinal fluid leaks. BSFs represent a significant linear blunt force and are independent predictors of mortality. LEVEL OF EVIDENCE: Prognostic and epidemiologic study, level III.

Infection rates, fevers, and associated factors in pediatric severe traumatic brain injury.

Abstract Infections can increase medical costs and worsen patient outcomes. Our aims in pediatric severe traumatic brain injury (sTBI) patients were to determine the infection and fever rates, and to report on associated clinical, imaging, treatment, and outcome factors. We included 180 sTBI patients (presedation Glasgow Coma Scale ≤ 8 and Maximum Abbreviated Injury Scale ≥ 4) admitted to our pediatric intensive care unit. Overall, 17% of sTBI patients (n=30 of 180) developed 36 infections, consisting primarily of urinary tract infections (UTIs; n=13 of 36) and ventilator-associated pneumonias (n=11 of 36). Most infections were nosocomial, occurring >2 days after admission. Fever was found in 36% of sTBI patients during the first few hospital days, but fewer than 7% of patients had infections. Infections occurred more frequently in sTBI patients who were older, heavier, and with a higher injury severity score (ISS; p<0.05). Admission head computed tomography imaging abnormalities (subarachnoid hemorrhage, intraventricular hemorrhage, and diffuse axonal injury), placement of an intracranial pressure (ICP) monitor, and administration of ICP-lowering therapies (hypertonic saline, mannitol, and thiopental) were associated with infections (p<0.05). Those with infections had fewer ventilator-free days, greater hospital lengths of stays, and were less likely to be discharged home. Logistic regression demonstrated that infections were independently associated with use of hypertonic saline (odds ratio [OR], 4.46; p=0.001) and higher ISS (OR, 1.05; p=0.028). In summary, infections were prevalent in sTBI patients and were associated with greater head-imaging abnormalities and use of ICP-lowering therapies. Hypertonic saline administration was strongly associated with infection, but further analyses are required to determine the nature of this relationship. Fever was a poor indicator of infection after sTBI.

The role of serious concomitant injuries in the treatment and outcome of pediatric severe traumatic brain injury.

BACKGROUND: The study objective was to describe the epidemiology of serious concomitant injuries and their effects on outcome in pediatric severe traumatic brain injury (sTBI). METHODS: A retrospective cohort of all severely injured (Injury Severity Score [ISS] ≥ 12) pediatric patients (<18 years) admitted to our pediatric intensive care unit, between 2000 and 2011, after experiencing an sTBI (Glasgow Coma Scale [GCS] score ≤ 8 and head Abbreviated Injury Scale [AIS] ≥ 4) were included. Two groups were compared based on the presence of serious concomitant injuries (maximum AIS score ≥ 3). Multivariate logistic regression was undertaken to determine variable associations with mortality. RESULTS: Of the 180 patients with sTBI, 113 (63%) sustained serious concomitant injuries. Chest was the most commonly injured extracranial body region (84%), with lung being the most often injured. Patients with serious concomitant injuries had increased age, weight, and injury severity (p < 0.001) and were more likely injured in a motor vehicle collision (91% vs. 48%, p < 0.001). Those with serious concomitant injuries had worse sTBI, based on lower presedation GCS (p = 0.031), higher frequency of fixed pupils (p = 0.006), and increased imaging abnormalities (SAH and DAI, p ≤ 0.01). Non-neurosurgical operations and blood transfusions were more frequent in the serious concomitant injury group (p < 0.01). The differences in mortality for the two groups failed to reach statistical significant (p = 0.053), but patients with serious concomitant injuries had higher rates of infection and acute central diabetes insipidus, fewer ventilator-free days, and greater length of stays (p < 0.05). Multivariate analyses revealed fixed pupillary response (odd ratio [OR], 63.58; p < 0.001), presedation motor GCS (OR, 0.23; p = 0.001), blood transfusion (OR, 5.80; p = 0.008), and hypotension (OR, 4.82; p = 0.025) were associated with mortality, but serious concomitant injuries was not (p = 0.283). CONCLUSION: Head injury is the most important prognostic factor in mortality for sTBI pediatric patients, but the presence of serious concomitant injuries does contribute to greater morbidity, including longer stays, more infections, fewer ventilator-free days, and a higher level of care required on discharge from hospital. LEVEL OF EVIDENCE: Prognostic and epidemiologic study, level III.

Hypernatremia is associated with increased risk of mortality in pediatric severe traumatic brain injury.

Acquired hypernatremia in hospitalized patients is often associated with poorer outcomes. Our aim was to evaluate the relationship between acquired hypernatremia and outcome in children with severe traumatic brain injury (sTBI). We performed a retrospective cohort study of all severely injured trauma patients (Injury Severity Score ≥12) with sTBI (Glasgow Coma Scale [GCS] ≤8 and Maximum Abbreviated Injury Scale [MAIS] ≥4) admitted to a Pediatric Critical Care Unit ([PCCU]; 2000-2009). In a cohort of 165 patients, 76% had normonatremia (135-150 mmol/L), 18% had hypernatremia (151-160 mmol/L), and 6% had severe hypernatremia (>160 mmol/L). The groups were similar except for lower GCS (p=0.002) and increased incidence of fixed pupil(s) on admission in both hypernatremia groups (p<0.001). Mortality rate was four-fold and six-fold greater with hypernatremia and severe hypernatremia, respectively (p<0.001), and mortality rates were unchanged when patients with fixed pupils or those with central diabetes insipidus were excluded (p<0.001). Hypernatremic patients had fewer ventilator-free days (p<0.001). Survivors with hypernatremia had greater PCCU (p=0.001) and hospital (p=0.031) lengths of stays and were less frequently discharged home (p=0.008). Logistic regression analyses of patient characteristics and sTBI interventions demonstrated that hypernatremia was independently associated with the presence of fixed pupil(s) on admission (odds ratio [OR] 5.38; p=0.003); administration of thiopental (OR 8.64; p=0.014), and development of central diabetes insipidus (OR 5.66; p=0.005). Additional logistic regression analyses demonstrated a significant association between hypernatremia and mortality (OR 6.660; p=0.034). In summary, acquired hypernatremia appears to signal higher risk of mortality in pediatric sTBI and is associated with a higher discharge level of care in sTBI survivors.